Crystal structure of coxsackievirus A9

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Molecular epidemiology and evolution of coxsackievirus A9.

Genetic relationships between 35 clinical isolates of coxsackievirus A9 (CAV9), collected during the last five decades from different geographical regions, were investigated by partial sequencing. Analysis of a 150 nucleotide sequence at the VP1/2A junction region identified 12 CAV9 genotypes. While most of the strains within each genotype showed geographical clustering, the analysis also provi...

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Degradation of coxsackievirus type A9 by proteolytic enzymes.

The means by which coxsackievirus type A9 (CA9) is inactivated by proteolytic enzymes was investigated. After reaction of (14)C-leucine-labeled CA9 with Pronase, free leucine was liberated as measured by radiochromatography. Treatment of (14)C-leucine-labeled CA9 with trypsin or proteolytic filtrates of Pseudomonas aeruginosa caused the release of a variety of labeled substances. The extent of ...

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Treatment of Coxsackievirus A9 myocarditis in mice with WIN 54954.

The therapeutic efficacy of an experimental antiviral agent, WIN 54954, was evaluated in murine myocardial infection with coxsackievirus A9 (CVA9). Eight-month-old male Swiss Webster mice were inoculated with 1.5 x 10(4) PFU of CVA9, Boston strain 13. WIN 54954, a broad-spectrum antipicornavirus agent, was administered orally in a dose of 0.25, 2.5, 25, 50, 100, or 200 mg/kg of body weight per ...

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Coxsackievirus A9 infects cells via nonacidic multivesicular bodies.

UNLABELLED Coxsackievirus A9 (CVA9) is a member of the human enterovirus B species in the Enterovirus genus of the family Picornaviridae. According to earlier studies, CVA9 binds to αVβ3 and αVβ6 integrins on the cell surface and utilizes β2-microglobulin, dynamin, and Arf6 for internalization. However, the structures utilized by the virus for internalization and uncoating are less well underst...

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Multiplication of Boston Strains of Coxsackievirus A9 in the Adult Mouse Heart.

Strains of coxsackievirus group A type 9 were isolated in Boston from 1959 through 1961 from patients with rash, aseptic meningitis, or pneumonia (Table 1). One of these strains (no. 13) multiplied in the myocardium of 7to 12-monthold mice, producing focal myocarditis (Lerner et al., New Engl. J. Med. 269:678, 736, 1963; Lerner, Levin, and Finland, J. Exptl. Med. 115: 745, 1962; Lerner, Progr. ...

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ژورنال

عنوان ژورنال: Seibutsu Butsuri

سال: 2000

ISSN: 0582-4052,1347-4219

DOI: 10.2142/biophys.40.s28_4